| First Author | Lin CH | Year | 2016 |
| Journal | Kidney Int | Volume | 89 |
| Issue | 6 | Pages | 1281-92 |
| PubMed ID | 27165830 | Mgi Jnum | J:315848 |
| Mgi Id | MGI:6832068 | Doi | 10.1016/j.kint.2016.01.030 |
| Citation | Lin CH, et al. (2016) Endostatin and transglutaminase 2 are involved in fibrosis of the aging kidney. Kidney Int 89(6):1281-92 |
| abstractText | Endostatin (EST), an antiangiogenic factor, is enriched in aging kidneys. EST is also an interactive partner of transglutaminase 2 (TG2), an enzyme that cross-links extracellular matrix proteins. Here we tested whether EST and TG2 play a role in the fibrosis of aging. In wild-type mice, aging kidneys exhibited a 2- to 4-fold increase in TG2 paralleled by increased cross-linked extracellular matrix proteins and fibrosis. Mice transgenic to express EST showed renal fibrosis at a young age. One-month delivery of EST via minipumps to young mice showed increased renal fibrosis that became more robust when superimposed on folic acid-induced nephropathy. Upregulated TG2 and impaired renal function were apparent with EST delivery combined with folic acid-induced nephropathy. Subcapsular injection of TG2 and/or EST into kidneys of young mice not only induced interstitial fibrosis, but also increased the proportion of senescent cells. Thus, kidney fibrosis in aging may represent a natural outcome of upregulated EST and TG2, but more likely it appears to be a result of cumulative stresses occurring on the background of synergistically acting geronic (aging) proteins, EST and TG2. |
